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| http://purl.uniprot.org/citations/18316610 | http://www.w3.org/2000/01/rdf-schema#comment | "The conversion of transforming growth factor beta (TGF-beta) from a tumor suppressor to a tumor promoter occurs frequently during mammary tumorigenesis, yet the molecular mechanisms underlying this phenomenon remain undefined. We show herein that TGF-beta repressed nuclear factor-kappaB (NF-kappaB) activity in normal NMuMG cells, but activated this transcription factor in their malignant counterparts, 4T1 cells, by inducing assembly of TGF-beta-activated kinase 1 (TAK1)-binding protein 1 (TAB1):I kappaB kinase beta (IKK beta) complexes, which led to the stimulation of a TAK1:IKK beta:p65 pathway. TAB1:IKK beta complexes could only be detected in NMuMG cells following their induction of epithelial-mesenchymal transition (EMT), which, on TGF-beta treatment, activated NF-kappaB. Expression of a truncated TAB1 mutant [i.e., TAB1(411)] reduced basal and TGF-beta-mediated NF-kappaB activation in NMuMG cells driven to undergo EMT by TGF-beta and in 4T1 cells stimulated by TGF-beta. TAB1(411) expression also inhibited TGF-beta-stimulated tumor necrosis factor-alpha and cyclooxygenase-2 expression in 4T1 cells. Additionally, the ability of human MCF10A-CA1a breast cancer cells to undergo invasion in response to TGF-beta absolutely required the activities of TAK1 and NF-kappaB. Moreover, small interfering RNA-mediated TAK1 deficiency restored the cytostatic activity of TGF-beta in MCF10A-CA1a cells. Finally, expression of truncated TAB1(411) dramatically reduced the growth of 4T1 breast cancers in syngeneic BALB/c, as well as in nude mice, suggesting a potentially important role of NF-kappaB in regulating innate immunity by TGF-beta. Collectively, our findings have defined a novel TAB1:TAK1:IKK beta:NF-kappaB signaling axis that forms aberrantly in breast cancer cells and, consequently, enables oncogenic signaling by TGF-beta."xsd:string |
| http://purl.uniprot.org/citations/18316610 | http://purl.org/dc/terms/identifier | "doi:10.1158/0008-5472.can-07-3094"xsd:string |
| http://purl.uniprot.org/citations/18316610 | http://purl.uniprot.org/core/author | "Schiemann W.P."xsd:string |
| http://purl.uniprot.org/citations/18316610 | http://purl.uniprot.org/core/author | "Neil J.R."xsd:string |
| http://purl.uniprot.org/citations/18316610 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18316610 | http://purl.uniprot.org/core/name | "Cancer Res"xsd:string |
| http://purl.uniprot.org/citations/18316610 | http://purl.uniprot.org/core/pages | "1462-1470"xsd:string |
| http://purl.uniprot.org/citations/18316610 | http://purl.uniprot.org/core/title | "Altered TAB1:I kappaB kinase interaction promotes transforming growth factor beta-mediated nuclear factor-kappaB activation during breast cancer progression."xsd:string |
| http://purl.uniprot.org/citations/18316610 | http://purl.uniprot.org/core/volume | "68"xsd:string |
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